Normal growth and its disorders

2020 ◽  
pp. 2416-2428
Author(s):  
Gary Butler

Normal growth has three phases: rapid in infancy and adolescence, steady during mid childhood. Height should always be interpreted within the context of the family: short or tall stature is often familial; idiopathic short stature occurs when the height of a normal child is below their target range. Constitutional growth delay is a common normal variant, but poor growth and/or weight gain may be associated with recognized and unrecognized chronic disease, and also with psychosocial deprivation. Investigation must exclude conditions including hypothyroidism, coeliac disease, inflammatory bowel disease, and chronic kidney disease. Turner syndrome (karyotype 45,X) should be suspected in all girls presenting with growth failure, and skeletal dysplasia when a child is either short for their family or has one parent of significant short stature.

Author(s):  
Gary Butler

Normal growth has three phases: rapid in infancy and adolescence, steady during mid childhood. Height should always be interpreted within the context of the family: short or tall stature is often familial; idiopathic short stature occurs when the height of a normal child is below their target range....


Author(s):  
Manuela Caruso-Nicoletti ◽  
V. De Sanctis ◽  
L. Cavallo ◽  
G. Raiola ◽  
L. Ruggiero ◽  
...  

AbstractShort stature is present in a significant percentage of patients affected by β-thalassaemia major. Growth failure of patients with thalassaemia is multifactorial. The most important contribution is attributed to the toxic effect desferrioxamine and to endocrine disorders, due to iron overload. The commonest endocrine complication is hypogonadism. The growth pat- tern of patients with thalassaemia is characterized by normal growth during childhood, a deceleration of growth velocity around age 9-10 years, and a reduced pubertal growth spurt. In addition, reduced growth of the trunk is often present. Short stature and short trunk are more evident at pubertal age. Hypogonadism is usually considered responsible for the pubertal growth failure, as well as the aggravation of body disproportion at pubertal age. However, data suggest that pubertal height gain and final height are reduced in both patients with spontaneous puberty and patients with induced puberty. It is concluded that several aspects of peripubertal growth in patients with thalassaemia remain to be clarified.


2020 ◽  
Vol 8 (1) ◽  
pp. 32-36
Author(s):  
Imthyas Khan V.H ◽  
Harshini B P ◽  
Ashoka C ◽  
Kumar G V

Background: Short stature is a term applied to a child whose height is two standard deviations or more below the mean height for children of that gender and chronologic age.Familial short stature and Constitutional Growth delay are considered as normal variants, the pathological short stature includes a wide variety of underlying disorders.Chronic systemic disorders, malnutrition, chromosomal or endocrinal disorders lead to a proportionate short stature.While most of the disproportionate short stature are secondary to skeletal dysplasias or resistant rickets.Etiological evaluation plays an important role in identification of physiological as well as pathological causes of short stature.Subjects and Methods:All children of age between 2 and 18 years with height below 2 standard deviation of mean for age and gender were included in the study. Result:A total of 100 children were studied who fulfilled the criteria of short stature, out of which 61 children were male and 39 were female children.Present study showed that females had more pathological variants (72%) than males (46%) whereas males had more physiological variants (54%) than females (28%) with P-value: 0.011Hypothyroidism was more common in females than males with 28% and 8% respectively. Genetic syndrome was more common in females than males with 10% and 3% respectively. Conclusion:Etiological evaluation is of pivotal role in identification of physiological as well as pathological causes of short stature and also helps in modifying the course of stature by means of early intervention.


2020 ◽  
Vol 7 (2) ◽  
pp. 363
Author(s):  
Muhammad Rezaul Karim ◽  
Kohinoor Jahan Shamaly ◽  
Baraka Badrudduja Tithi ◽  
Romana Akter ◽  
Ismat Jahan ◽  
...  

Background: Short stature is a common problem to practicing pediatricians. It results from various etiologies, which are categorized as normal variants and pathological causes. Normal variant short stature consists of Familial Short Stature (FSS) and Constitutional Growth Delay (CGD), while pathological causes are subdivided into endocrine diseases, clinically defined syndromes, chronic diseases, metabolic diseases and others. There are not so much data available in Bangladesh in this respect. So, present study was conducted to know the common causes of short stature.Methods: This cross-sectional study was done in pediatric endocrinology clinic of Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh from January 2017 to August 2018. One hundred children with short stature meeting inclusion criteria were recruited after taking an informed consent. The detailed history, physical examination including anthropometric measurements and relevant investigations were done. Data were recorded on a predesigned questionnaire for final analysis.Results: The common causes of short stature identified were familial short stature (FSS) 51% cases, Constitutional Growth Delay (CGD) 14% cases and hypothyroidism 12% cases. Other less common causes of short stature were Growth Hormone Deficiency (GHD) 8% cases, malnutrition 6% cases and genetic syndrome 5% cases.Conclusions: FSS and CGD were the leading cause of short stature in children. Endocrinological causes were the most common cause of short stature after normal variant while nonendocrine causes were the least.


1986 ◽  
Vol 113 (4_Suppl) ◽  
pp. S24-S28 ◽  
Author(s):  
KAREN ARMOUR ◽  
STUART CHALEW ◽  
A. AVINOAM KOWARSKI

Abstract Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1+1.7 μg/dl; mean±ISD) which exceeded the IC-F in healthy children and adults (5.7±1.5 μg/dl; P<0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2±4.7 μg/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.


2020 ◽  
Vol 33 (10) ◽  
pp. 1335-1339
Author(s):  
Sayaka Kawashima ◽  
Hiroko Yagi ◽  
Yasuhiro Hirano ◽  
Machiko Toki ◽  
Kei Izumi ◽  
...  

AbstractObjectivesImprinted genes have important roles for normal growth and development. Imprinting disorders (IDs) such as Silver-Russell syndrome and Temple syndrome are rare diseases that typically cause short children born small for gestational age (SGA). However, some patients with short stature (SS) caused by IDs were born non-SGA. To date, the contribution of IDs to idiopathic short stature (ISS) has been poorly investigated. The aim of this study was to clarify the contribution of IDs to ISS.MethodsWe conducted methylation analysis for 10 differentially methylated regions using pyrosequencing to detect known IDs in 58 patients (31 male and 27 female children, height standard deviation score −4.2 to −2.0) carrying a clinical diagnosis of ISS.ResultsWe identified no patient with IDs among these patients with ISS.ConclusionsThese results indicate that IDs are rare in patients having ISS, and that imprinted genes affect fetal growth more than postnatal growth. Because patients with IDs born non-SGA usually have clinical features characteristic of each ID, in addition to SS, the patients with ISS as a clinical diagnosis may not be associated with IDs.It is unlikely that cases clinically diagnosed with ISS are caused by IDs leading to growth failure.


2021 ◽  
pp. 1-3
Author(s):  
Christina N.  Katsagoni

Growth delay with height and weight impairment is a common feature of pediatric inflammatory bowel diseases (PIBD). Up to 2/3 of Crohn Disease patients have impaired weight at diagnosis, and up to 1/3 have impaired height. Ulcerative colitis usually manifests earlier with less impaired growth, though patients can be affected. Ultimately, growth delay, if not corrected, can reduce final adult height. Weight loss, reduced bone mass, and pubertal delay are also concerns associated with growth delay in newly diagnosed PIBD patients. The mechanisms for growth delay in IBD are multifactorial and include reduced nutrient intake, poor absorption, increased fecal losses, as well as direct effects from inflammation and treatment modalities. Management of growth delay requires optimal disease control. Exclusive enteral nutrition (EEN), biologic therapy, and corticosteroids are the primary induction strategies used in PIBD, and both EEN and biologics positively impact growth and bone development. Beyond adequate disease control, growth delay and pubertal delay require a multidisciplinary approach, dependent on diligent monitoring and identification, nutritional rehabilitation, and involvement of endocrinology and psychiatry services as needed. Pitfalls that clinicians may encounter when managing growth delay include refeeding syndrome, obesity (even in the setting of malnutrition), and restrictive diets. Although treatment of PIBD has improved substantially in the last several decades with the era of biologic therapies and EEN, there is still much to be learned about growth delay in PIBD in order to improve outcomes.


2021 ◽  
pp. 115-120
Author(s):  
Melanie Ribau ◽  
Mário Baptista ◽  
Nuno Oliveira ◽  
Bruno Direito Santos ◽  
Pedro Varanda ◽  
...  

Partial physeal bars may develop after injury to the growth plate in children, eventually leading to disturbance of normal growth. Clinical presentation, age of the patient, and the anticipated growth will dictate the best treatment strategy. The ideal treatment for a partial physeal bar is complete excision to allow growth resumption by the remaining healthy physis. There are countless surgical options, some technically challenging, that must be weighted according to each case’s particularities. We reviewed the current literature on physeal bars while reporting the challenging case of a short stature child submitted to a femoral physeal bar endoscopic-assisted resection with successful growth resumption. This case dares surgeons to consider all options when treating limb length discrepancy, such as the endoscopic-assisted resection which might offer successful results.


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